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Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226
We tested the hypothesis that
nitric oxide (NO) inhibits endothelium-derived hyperpolarizing factor
(EDHF)-induced vasodilation via a negative feedback pathway in the
coronary microcirculation. Coronary microvascular diameters were
measured using stroboscopic fluorescence microangiography. Bradykinin
(BK)-induced dilation was mediated by EDHF, when NO and prostaglandin
syntheses were inhibited, or by NO when EDHF and prostaglandin
syntheses were blocked. Specifically, BK (20, 50, and 100 ng · kg
1 · min1 ic) caused dose-dependent
vasodilation similarly before and after administration of
NG-monomethyl-L-arginine
(L-NMMA) (3 µmol/min ic for 10 min) and indomethacin (Indo, 10 mg/kg iv). The residual dilation to BK with
L-NMMA and Indo was completely abolished by suffusion of miconazole or an isosmotic buffer containing high KCl (60 mM), suggesting that this arteriolar vasodilation is mediated by the cytochrome P-450 derivative EDHF. BK-induced dilation was
reduced by 39% after inhibition of EDHF and prostaglandin synthesis,
and dilation was further inhibited by combined blockade with
L-NMMA to a 74% reduction in the response. This suggests
an involvement for NO in the vasodilation. After dilation to BK was
assessed with L-NMMA and Indo, sodium nitroprusside (SNP,
1-3 µg · kg1 · min1
ic), an exogenous NO donor, was administered in a dose to increase the
diameter to the original control value. Dilation to BK was virtually
abolished when administered concomitantly with SNP during L-NMMA and Indo (P < 0.01 vs. before SNP),
suggesting that NO inhibits EDHF-induced dilation. SNP did not affect
adenosine- or papaverine-induced arteriolar dilation in the presence of
L-NMMA and Indo, demonstrating that the effect of SNP was
not nonspecific. In conclusion, our data are the first in vivo evidence
to suggest that NO inhibits the production and/or action of EDHF in the
coronary microcirculation.
endothelium-derived hyperpolarizing factor; endothelium-dependent dilation; coronary microcirculation
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